Prostaglandin Signaling Stimulates Tumor Growth

They reported in the September 2004 issue of Cancer Cell that treatment of the animals with PGE2 caused an increase in polyp number and size. The effect of PGE2 was linked to activation of the cell apoptosis regulator peroxisome proliferator-activated receptor d (PPARd). Mice genetically engineered to lack PPARd did not show increased polyp formation after PGE2 treatment.

"Our results identify PPARd as a critical downstream mediator in PGE2-stimulated promotion of colorectal tumor growth,” said senior author Dr. Raymond N. DuBois, professor of medicine at Vanderbilt University. "They suggest that PPARd is an important pro-cancer factor in CRC, and that agents which stimulate PPARd may encourage abnormal cell growth in certain populations at risk for CRC. In addition, it is possible that blocking PPARd might prove useful for prevention and/or treatment of CRC.”



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